Kernicterus

Introduction Bilirubin encephalopathy is caused by increased bilirubin in the blood, mainly unbound bilirubin, which enters the central nervous system and causes lesions in the basal ganglia, hypothalamic nucleus, globus pallidus, etc., serum bilirubin. >342umol/L (20mg/dl) is at risk of developing nuclear jaundice. Mainly manifested as severe jaundice muscle tension is too low or too high, lethargy, refusal to milk, rigidity, angulation, convulsions and so on. The disease is mostly caused by hemolytic disease of the newborn (maternal and infant blood type is not the most, G-6PD defect is second), jaundice, severe anemia is easy to be complicated by bilirubin encephalopathy, if bilirubin encephalopathy has occurred, the treatment effect is not Good, the consequences are serious, and it is easy to leave behind the sequelae of mental retardation, hand and foot movement, hearing impairment, convulsions. Therefore, prevention of this disease is the key. Found that neonatal jaundice, should go to the hospital as soon as possible to prevent the disease.

Cause

Bilirubin can bind tightly to serum albumin and cannot pass freely through the blood-brain barrier. As long as there is a bilirubin binding site on albumin, it will not cause nuclear jaundice. Significantly elevated serum bilirubin, low serum albumin concentration or substances in the serum that compete with bilirubin for albumin binding sites, such as free fatty acids, hydrogen ions, certain drugs including sulfa drugs, cephalosporins and aspirin, Both can increase the risk of nuclear jaundice. Premature babies are at risk of nuclear jaundice due to low serum albumin concentrations. In neonatal serum of hunger, sepsis, respiratory distress or metabolic acidosis, competitive molecules (such as free fatty acids and hydrogen ions) may be elevated, which increases the number of newborns at any serum bilirubin level. The danger of jaundice.

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Early symptoms of full-term infants are lethargy, poor milk and vomiting, followed by angulation, eye gaze, convulsions and death. In preterm infants, nuclear jaundice may not exhibit recognizable clinical signs. Nuclear jaundice can lead to post-child mental retardation, hand-foot-like cerebral palsy, sensorineural hearing loss and paralysis of the eye gaze, and it is not clear whether the degree of bilirubin encephalopathy can reduce the damage of the nervous system (eg Perception - dyskinesia and learning difficulties).

There is no reliable experiment to determine the risk of developing a nuclear jaundice in a newborn, and the diagnosis is through autopsy.

Differential diagnosis

Symptoms of nuclear jaundice need to be differentiated from the following symptoms:

Severe jaundice: Astragalus, also known as jaundice, commonly known as yellow rickets, is a symptom and sign of yellowing of the skin, mucous membranes and sclera due to elevated serum bilirubin. Certain liver diseases, gallbladder diseases, and blood diseases often cause symptoms of jaundice. Usually, when the blood bilirubin concentration is higher than 2-3 mg/dL (34-51), these parts will have a color that can be discerned by the naked eye. Recessive jaundice: 17~34, mild jaundice: 34~170, moderate jaundice: 170~340, severe jaundice: >340.

Pathological jaundice: Astragalus is common in newborns at any other age, and its etiology is special and complex, both physiological jaundice, pathological jaundice, and breast milk jaundice. These situations should be treated differently and handled. If the child develops jaundice or jaundice within 24 hours after birth, it will develop too fast and last for a long time, even with anemia, abnormal body temperature, poor feeding, vomiting, and abnormal color of urine and urine. Some are yellow sputum that has subsided or reduced and then reappeared and aggravated, mostly pathological jaundice. Common causes of pathological jaundice are neonatal hemolytic disease, neonatal infection, biliary malformation, and neonatal hepatitis.

Physiological jaundice: Astragalus is a common clinical symptom in the neonatal period. Because of its different pathogenesis, it can be either a physiological phenomenon or a pathological phenomenon. Clinically, the total serum bilirubin in term infants exceeds 205.2 mol/L (12 mg/dl), and the preterm infants exceed 256.5 mol/L (15 mg/dl) is called hyperbilirubinemia.

Neonatal jaundice after breastfeeding: breast-fed infants develop jaundice 4 to 7 days after birth, peak at 2 to 4 weeks (serum bilirubin can exceed 256.6-342.0 mol/L), generally in good condition without hemolysis or anemia The performance of jaundice usually lasts for 3 to 4 weeks, and gradually disappears in the second month. A few can be extended to 10 weeks before the jaundice is stopped. If the breast milk is stopped for 3 to 4 days, the jaundice is obviously reduced, and the bilirubin is reduced by 50%. Feeding, jaundice does not necessarily appear again, even if it does not reach the original level.

Hemolytic jaundice: Any disease that causes hemolysis can produce hemolytic jaundice.

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